ArticleThe American journal of pathology2000
In situ localization of C3 synthesis in experimental acute renal allograft rejection.
Article in The American journal of pathology, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT03791476 (A Phase I/II,Single Center,Randomized,Double-Blind,Placebo-Controlled Study to Evaluate the Feasibility of Using Human Recombinant C1 Inhibitor), which is not on this map. Cited by 34 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
A Phase I/II,Single Center,Randomized,Double-Blind,Placebo-Controlled Study to Evaluate the Feasibility of Using Human Recombinant C1 Inhibitor(RUCONEST®) as a Therapeutic Strategy to Reduce the Incidence of Delayed Graft Function in Recipients of Kidneys From Donation After Cardio-Circulatory Death
Who cites it
34 citing papers in PubMed, 78 citations in OpenAlex.
- Mitochondria: The Crossroads of Complement Activation and Kidney Injury Progression.International journal of molecular sciences · 2026Review
- Complement activation in kidney transplantation.Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association · 2026Review
- Critical role of complement in antibody mediated rejection in kidney transplantation.World journal of transplantation · 2025Review
- The secret life of complement: challenges and opportunities in exploring functions of the complosome in disease.The Journal of clinical investigation · 2025Review
- Role of intrarenal complement production in kidney transplantation.Clinical kidney journal · 2025Review
- Article
- Review
- The state of complement in COVID-19.Nature reviews. Immunology · 2022Review
- Article
- The Contribution of Complement to the Pathogenesis of IgA Nephropathy: Are Complement-Targeted Therapies Moving from Rare Disorders to More Common Diseases?Journal of clinical medicine · 2021Review
- Renal diseases and the role of complement: Linking complement to immune effector pathways and therapeutics.Advances in immunology · 2021Review
- Inflammaging and Complement System: A Link Between Acute Kidney Injury and Chronic Graft Damage.Frontiers in immunology · 2020Review
- Post-transplant Alternative Complement Pathway Activation Influences Kidney Allograft Function.Archivum immunologiae et therapiae experimentalis · 2019Article
- Complement-mediated Damage to the Glycocalyx Plays a Role in Renal Ischemia-reperfusion Injury in Mice.Transplantation direct · 2019Article
- Article
- Update on ischemia-reperfusion injury in kidney transplantation: Pathogenesis and treatment.World journal of transplantation · 2015Review
- Complement involvement in kidney diseases: From physiopathology to therapeutical targeting.World journal of nephrology · 2015Review
- The complement cascade and renal disease.Archivum immunologiae et therapiae experimentalis · 2014Review
- The role of complement in the pathogenesis of renal ischemia-reperfusion injury and fibrosis.Fibrogenesis & tissue repair · 2014Review
- The innate immune system and transplantation.Cold Spring Harbor perspectives in medicine · 2013Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Recent evidence has implicated complement in renal transplant injury and identified the kidney as a source of complement components. We therefore investigated the local gene expression of complement component C3, pivotal to complement activation pathways and a mediator of inflammatory injury, in a rat renal transplant model. By reverse transcriptase-polymerase chain reaction, the expression of C3 mRNA increased in two phases. The first phase coincided with post-ischemic injury over 2 days post-transplantation and was localized by in situ hybridization to vessels and glomerular mesangial cells in allogeneic and syngeneic (control) kidney transplants. In allografts only, a second phase was found in tubular epithelial cells, glomerular parietal cells, vessel walls and some infiltrating cells, which peaked on day 4 together with rapid influx of leukocytes, tubule cell damage, the induction of interleukin-2 and interferon-gamma mRNA, and the up-regulation of tumor necrosis factor-alpha and interleukin-1beta mRNA in the graft. In vitro studies showed that interleukin-2 and interferon-gamma up-regulate C3 production in renal tubule cells. We conclude that post-ischemic injury led to transient up-regulation of glomerular expression of C3 mRNA. Subsequent cellular rejection was associated with tubulointerstitial/glomerular parietal cell expression of C3 mRNA. This differential expression of local C3, immediately post-transplant or associated with acute rejection, may have implications for putative therapeutic complement inhibition in clinical transplantation.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.